HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 288/6/H2785    most recent 00354.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (11) Citing Articles via Google Scholar Google Scholar Articles by Damon, D. H. Search for Related Content PubMed PubMed Citation Articles by Damon, D. H.

Sympathetic innervation promotes vascular smooth muscle differentiation

Department of Pharmacology, University of Vermont, Burlington, Vermont

Submitted 13 April 2004 ; accepted in final form 16 January 2005

The sympathetic nervous system (SNS) is an important modulator of vascular smooth muscle (VSM) growth and function. Several lines of evidence suggest that the SNS also promotes VSM differentiation. The present study tests this hypothesis. Expression of smooth muscle myosin (SM2) and -actin were assessed by Western analysis as indexes of VSM differentiation. SM2 expression (normalized to -actin) in adult innervated rat femoral and tail arteries was 479 ± 115% of that in noninnervated carotid arteries. Expression of -actin (normalized to GAPDH or total protein) in 30-day-innervated rat femoral arteries was greater than in corresponding noninnervated femoral arteries from guanethidine-sympathectomized rats. SM2 expression (normalized to -actin) in neonatal femoral arteries grown in vitro for 7 days in the presence of sympathetic ganglia was greater than SM2 expression in corresponding arteries grown in the absence of sympathetic ganglia. In VSM-endothelial cell cultures grown in the presence of dissociated sympathetic neurons, -actin (normalized to GAPDH) was 300 ± 66% of that in corresponding cultures grown in the absence of neurons. This effect was inhibited by an antibody that neutralized the activity of transforming growth factor-2. All of these data indicate that sympathetic innervation increased VSM contractile protein expression and thereby suggest that the SNS promotes and/or maintains VSM differentiation.

endothelial cells; transforming growth factor-; -actin; myosin

This article has been cited by other articles:

				D. H. Damon TH and NPY in sympathetic neurovascular cultures: role of LIF and NT-3 Am J Physiol Cell Physiol, January 1, 2008; 294(1): C306 - C312. [Abstract] [Full Text] [PDF]

				D. H. Damon, J. A. teRiele, and S. B. Marko Vascular-derived artemin: a determinant of vascular sympathetic innervation? Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H266 - H273. [Abstract] [Full Text] [PDF]

				P. J. Mueller Exercise training attenuates increases in lumbar sympathetic nerve activity produced by stimulation of the rostral ventrolateral medulla J Appl Physiol, February 1, 2007; 102(2): 803 - 813. [Abstract] [Full Text] [PDF]

				T. Schluter, R. Grimm, A. Steinbach, G. Lorenz, R. Rettig, and O. Grisk Neonatal sympathectomy reduces NADPH oxidase activity and vascular resistance in spontaneously hypertensive rat kidneys Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2006; 291(2): R391 - R399. [Abstract] [Full Text] [PDF]